Decreased fucosylation impacts epithelial integrity and increases risk for COPD.

ABSTRACT: COPD causes significant morbidity and mortality worldwide. Epithelial damage is fundamental to disease pathogenesis, although the mechanisms driving disease remain undefined. Published evidence from a COPD cohort (SPIROMICS) and confirmed in a second cohort (COPDgene) demonstrate a polymorphism in Fucosyltransferese-2 (FUT2) is a trans-pQTL for E-cadherin, which is critical in COPD pathogenesis. We found by MALDI-TOF analysis that FUT2 increased terminal fucosylation of E-cadherin. Using atomic force microscopy, we found that FUT2-dependent fucosylation enhanced E-cadherin-E-cadherin bond strength, mediating the improvement in monolayer integrity. Tracheal epithelial cells from Fut2^-/- mice have reduced epithelial integrity, which is recovered with re

SUBMITTER: Swaby C 

PROVIDER: S-EPMC10635007 | biostudies-literature | 2023 Nov

REPOSITORIES: biostudies-literature